GPR7

GPR7, currently designated neuropeptide B/W receptor 1 (NPBWR1), is a class A G protein-coupled receptor that mediates signaling initiated by the endogenous neuropeptides neuropeptide B (NPB) and neuropeptide W (NPW) and is predominantly expressed in the central nervous system^[1][2]. Mechanistically, GPR7 participates in neuropeptide-dependent GPCR signaling pathways that regulate feeding behavior, energy homeostasis, neuroendocrine activity, stress responses, and inflammatory pain processing^[1][3]. Through activation by NPB and NPW, this receptor contributes to coordinated control of metabolic and neuroendocrine functions, linking central neuronal signaling with systemic physiological regulation^[1][2]. In experimental studies, disruption or downregulation of the NPB/GPR7 signaling axis has been associated with increased adiposity and metabolic alterations, supporting its relevance as a model system for investigating energy balance and obesity-related mechanisms^[1]. Compared with the related isoform NPBWR2 (GPR8), GPR7 displays a distinct species distribution because NPBWR2 is absent in rodents, making GPR7 the principal receptor mediating NPB/NPW signaling in commonly used rodent models^[1][2]. This distinction has increased the value of GPR7 for translational studies examining neuropeptide-regulated metabolism and neuroendocrine function^[1][2]. For experimental applications, stable and potent NPBWR1 agonists have been developed through peptidomimetic optimization, providing pharmacological tools for receptor activation studies and mechanistic investigation of GPR7-dependent signaling pathways^[4].